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Twenty-four distinct outbreaks of probable chikungunya (CHIK) etiology were identified throughout Indonesia from September 2001 to March 2003, after a near 20-year hiatus of epidemic CHIK activity in the country. Thirteen outbreak reports were based on clinical observations alone, and 11 confirmed by serological/virological methods. Detailed epidemiological profiles of two investigated outbreaks in Bogor and Bekasi are presented. Human sera were screened using an ELISA for IgM and IgG anti-CHIK antibodies. Additionally, reverse transcriptase PCR and virus isolation were attempted for virus identification. The mean age of cases was 37 +/- 18 years in Bogor and 33 +/- 20 years in Bekasi. There was no outstanding case-clustering, although outbreak-affected households were observed to be geographically grouped within villages. The attack rates in Bogor and Bekasi were 2.8/1000 and 6.7/1000 inhabitants respectively. Both outbreaks started in the rainy season following increased Aedes aegypti and A. albopictus densities.

Although influenza is recognized for its worldwide importance, little is known about the disease from tropical countries like Indonesia. From August 1999 through January 2003, a surveillance study was conducted in clinics at 6 sentinel locations. Adults (age, >14 years) and children (age, 4-14 years) presenting with respiratory symptoms suggestive of influenza were asked to enroll in the study. Nasal and pharyngeal swabs were examined by virus isolation, polymerase chain reaction, and rapid immunochromatographic tests. A total of 3079 specimens were collected from 1544 participants. Influenza infection was confirmed in 172 volunteers (11.1%) presenting with influenza-like illness. Influenza A (H1N1 and H3N2) and B viruses were detected at all sites. Peak prevalence tended to coincide with the respective rainy seasons, regardless of location. In light of the recent epidemic of severe acute respiratory syndrome, continued influenza surveillance would be useful in strengthening the infrastructure of the Indonesian public health system.

A suspected hepatitis outbreak occurred in Bondowoso District, East Java Province, Indonesia, in March-May 1998. An investigation was initiated in April 1998, involving a retrospective review of hospital records, a community-based cross-sectional study, and a health service-based case detection and household follow-up. Sera and epidemiological information were collected from 962 individuals: 235 from 3 outbreak-affected communities along the same rural stretch of river, 101 from community controls living distant from the river, 151 cases detected in health centres, 141 family members of the cases, and 334 subjects from neighbouring families. The prevalence of acute hepatitis E virus (HEV), based on anti-HEV IgM, total antibody (Ig) to HEV and polymerase chain reaction (PCR), was significantly (P < 0.00001) higher (52.4%) among the outbreak communities than among the community controls (3%). The background prevalence of HEV, based on anti-HEV IgG, was also significantly (P < 0.00001) higher (47%) among the outbreak communities than among the community controls (3%). None of the 476 sera screened for anti-HAV (hepatitis A virus) IgM was positive. These results indicate that HEV was the aetiological agent responsible for the outbreak. The overall attack rate (AR) for the 3 outbreak-affected communities surveyed was 19%, with AR determined on the basis of clinically recognized, acute jaundice illness. The usage of river water as primary source for bathing, human-waste disposal, and drinking purposes differed significantly (P < 0.00001) between the communities in outbreak areas and those in non-outbreak areas. There is no significant influence attributed to 'boiling water' on acute HEV. No climatic influences (flooding or drought) predisposed this instance of epidemic HEV transmission. This outbreak represents the first documented evidence of epidemic HEV transmission in Java, Indonesia.

An outbreak of dengue fever (DF), dengue haemorrhagic fever (DHF), and dengue shock syndrome (DSS) in the city of Palembang, south Sumatra, Indonesia was investigated to (i) validate epidemic occurrence, (ii) confirm dengue virus aetiology and associated serotype(s), (iii) provide a demonstrable measure of community impact, and (iv) identify causative relationship (if any) with climatic El Niño Southern Oscillation (ENSO) influences. Trend analysis based on a 6-year retrospective review of hospital records demonstrates a 3-fold increase in clinical cases for the outbreak period (January-April 1998), relative to historical records. In the 2 hospitals surveyed, the monthly mean number of outbreak-related dengue cases over 4 months was 833 (range 650-995 cases/month); the mean monthly value for the previous 72 months was 107 (range 14-779 cases/month). An apparent trend in epidemic transmission was observed, evolving from a 5-year cyclic phenomenon to an annual occurrence, often indistinguishable from one year to the next. The proportional distribution of clinical outbreak cases into DF, DHF and DSS diagnostic categories was 24%, 66%, and 10%, respectively. The population aged 10-19 years accounted for the largest (35%) proportion of hospitalized DHF cases, followed by children aged 5-9 years (25%) and children aged 4 years (16%). Serum samples obtained during acute illness from 221 hospitalized patients were examined using serology, RT-PCR, and virus isolation in cell culture: 59% of samples had laboratory evidence of a dengue infection. All 4 dengue virus serotypes (DEN 1-4) were identified in epidemic circulation, with DEN 3 predominating (43%). DEN 1 was the principal serotype associated with less severe dengue illness, suggesting that virulence may be, in part, a function of infecting serotype. The climatic influence of ENSO on rainfall and temperature in the months leading up to and during the outbreak was dramatic, and is likely to contribute to favourable outbreak conditions.

The ecology of hepatitis E virus (HEV) transmission in South-East Asia was assessed from a review of 6 published and 3 unpublished NAMRU-2 reports of hepatitis outbreak investigations, cross-sectional prevalence studies, and hospital-based case-control studies. Findings from Indonesia and Viet Nam show epidemic foci centred in jungle, riverine environments. In contrast, few cases of acute, clinical hepatitis from cities in Indonesia, Viet Nam and Laos could be attributed to HEV. When communities in Indonesia were grouped into areas of low (< 40%), medium (40-60%), and high (> 60%) prevalence of anti-HEV antibodies, uses of river water for drinking and cooking, personal washing, and human excreta disposal were all significantly associated with high prevalence of infection. Conversely, boiling of river drinking water was negatively associated with higher prevalence (P < 0.01). The protective value of boiling river water was also shown in sporadic HEV transmission in Indonesia and in epidemic and sporadic spread in Viet Nam. Evidence from Indonesia indicated that the decreased dilution of HEV in river water due to unusually dry weather contributed to risk of epidemic HEV transmission. But river flooding conditions and contamination added to the risk of HEV infection in Viet Nam. These findings attest to a unique combination of ecological and environmental conditions predisposing to epidemic HEV spread in South-East Asia.

Analysis of serum samples from patients with acute jaundice by means of enzyme-linked immunosorbent assay and polymerase chain reaction testing provided the first profile of this condition in Vientiane, Lao PDR, in 1995 and 1996. In a case-control, hospital-based study, evidence of acute infections due to hepatitis A and B viruses was found in 14% and 10% of cases, respectively. Hepatitis E virus, however, did not appear to contribute to clinically recognized acute jaundice. Similarly, antibody to hepatitis C virus was recognized in almost equal proportions of cases (8%) and controls (6%), thus representing probable background infections. The detection of hepatitis G virus marks the first report of this virus in Lao PDR. The large proportion (21%) of new leptospiral infections in cases without acute hepatitis A or B was notable. This finding suggests significant regional underreporting of leptospirosis as a cause of acute jaundice. The limited laboratory diagnostic capabilities for confirming a differential diagnosis of leptospirosis contribute to the lack of attention paid to this important health problem.

A suspected epidemic of unknown etiology was investigated in April/May 1996 in the remote jungle highlands of easternmost Indonesia. Trend analysis demonstrates the area-wide occurrence of a major respiratory infection outbreak in November 1995 through February 1996. The monthly mean rate of respiratory infection episodes for the peak outbreak months (2,477 episodes/100,000 persons) was significantly higher (P < .0001) than for the 34 months leading up to the outbreak (109 episodes/100,000 persons). Notable were the high attack rates, particularly among adults: 202 episodes/1,000 persons aged 20-50 years in one community. Excess morbidity attributed to the outbreak was an estimated 4,338 episodes. The overall case-fatality rate was 15.1% of outbreak cases. Laboratory evidence confirmed the circulation of influenza A/Taiwan/1/86-like viruses in the study population, and high hemagglutination inhibition titer responses were indicative of recent infections. Historical documents from neighboring Papua New Guinea highlight the role of influenza A virus in repeated area outbreaks.

A study of acute hepatitis was conducted in Hanoi, Viet Nam, from January 1993 to February 1995; 188 sera from clinical hepatitis cases were screened by enzyme-linked immunosorbent assay for immunoglobulin (Ig) M anti-hepatitis A virus (HAV), IgM anti-hepatitis B core antigen (HBc), IgG anti-hepatitis C virus (HCV), IgG anti-hepatitis E virus (HEV) and IgM anti-HEV. Additionally, 187 sera from control subjects, matched by age, sex and month of admission, with no recent history of hepatitis, were tested for comparative purposes. There was serological evidence of recent HAV (29%) and hepatitis B virus (24%) infection in 53% of cases (2 mixed infections), compared with 2% of controls. HCV infections were detected in 10% of cases (with no IgM anti-HAV or IgM anti-HBc) and in 1% of control sera. There was no significant difference in the proportion of IgG anti-HEV positive sera between cases (in the absence of IgM anti-HAV or IgM anti-HBc) (21%) and controls (14%); 3% of all case sera were IgM anti-HEV positive. Younger cases (< 20 years) were more likely to have recent HAV infections (41%) than those aged > or = 20 years (21%) (P < 0.01). In contrast, a higher percentage of adult cases had IgM anti-HBc, IgG anti-HCV and IgG anti-HEV (in the absence of recent HAV or HBV infection) than did children. No seasonal trend in hepatitis admissions was detected, nor an association between water-borne infections (HAV and HEV) and the warmer months. Hepatitis patients lived throughout Hanoi and surrounding areas, with no identifiable geographical clustering, regardless of serological marker.

The prevalence in Somalia of antibody to hepatitis C virus (anti-HCV) was determined in a survey of 236 female prostitutes, 80 sexually transmitted disease (STD) clinic patients, 79 male soldiers, and 43 tuberculosis patients. Of 98 (22%) serum samples repeatedly anti-HCV reactive by first and second generation enzyme-linked immunosorbent assay kits, only 8 (1.8%) were anti-HCV positive by immunoblot assay (RIBA-2). Anti-HCV seropositivity by immunoblot assay was not associated with any risk group or with positive syphilis serology (found in 18% of subjects) or antibody to human immunodeficiency virus 1 (in 1.4% of subjects). These data indicate that sexual transmission of hepatitis C virus is not common in Somalia among sexually active populations, including female prostitutes and other groups at high risk of STDs and the acquired immune deficiency syndrome.

In April 1991, 91 hospitalized patients in Cairo were reported to the Egyptian Ministry of Health with botulism intoxication. To define the spectrum of illness and identify a food vehicle, 45 patients were interviewed and a case-control investigation was conducted among families of 5 hospitalized patients. Clinical specimens and specimens of implicated food were tested for toxin and cultured for Clostridium botulinum. Hospitalized patients had symptoms consistent with botulism; 18 (20%) of 91 reported patients died. Illness was associated with eating faseikh (uneviscerated, salted mullet fish; lower 95% confidence limit of odds ratio = 6.6, P < .001). All 5 case-families purchased faseikh from one shop. Very high levels of type E botulinal toxin were detected in faseikh reported to be purchased from the implicated shop; C. botulinum type E was isolated from cultures of clinical specimens and from the faseikh. This is the first documented outbreak of botulism in Egypt and the largest type E outbreak ever reported.